GABA(A) alpha-1 subunit mediated desynchronization of elevated low frequency oscillations alleviates specific dysfunction in stroke – A case report

GABA-mediated changes in inter-hemispheric beta frequency activity in early-stage Parkinson’s disease

“…Zolpidem greatly reduced the synchronous power of pathological oscillations in these loci, which correlated well with zolpidem uptake and restoration of function. These results suggest that specific motor and cognitive impairments are related to increased low-frequency oscillatory neuronal network activity, and that zolpidem is able to desynchronize such pathological low-frequency activity, restoring cognitive and motor function (for further details see Hall et al, 2010b). …”

“…Muscle activity was recorded using electromyography (EMG) (Delsys, Boston, MA, USA) in the first dorsal interosseus (FDI) muscle, which controls index-finger abduction. At the end of the first recording session, participants were administered oral zolpidem (0.05 mg/kg), consistent with previously reported effective sub-sedative doses (Hall et al, 2010b). An identical second MEG recording session was initiated 50 min after the zolpidem administration, with participants required to repeat the same rest and movement periods.…”

“…Our own previous study with a brain-injured participant revealed persistent pathological theta (4–10 Hz) and beta (15–35 Hz) oscillations in cortical areas surrounding the lesion (Hall et al, 2010b). Specifically, sensorimotor and language areas exhibited pathological beta and theta, consistent with altered gait and speech agnosia.…”

The role of GABAergic modulation in motor function related neuronal network activity

“…The influence of diazepam on the MRBD, specifically increasing the level of desynchronisation, provides an important focus for investigating the role of GABAergic modulation in motor function. Particularly, as recent studies have demonstrated that abnormally elevated beta oscillations in M1 appear to be directly related to impaired motor function in stroke (Hall et al, 2010b).…”

Blood-brain barrier integrity in a zolpidem-responder patient

“…3 These dormant areas have no typical location, vary from patient to patient and have slow-wave rhythmic electrical activity which desynchronises after zolpidem treatment. 4 Neurotransmitter abnormalities, including γ-aminobutyric acid (GABA) depletion via chronic blood-brain barrier (BBB) dysfunction, have been proposed as the cause for dormancy. Other considerations include leakage into the cerebrospinal fluid or inadequate neurotransmitter production.…”